It has been revealed that the change of miRNA expressions contributes to the initiation and progression of cancer. More than 50% of miRNAs are located in cancer-associated genomic regions or in fragile sites (5). The expression of miR-15a and miR-16, which locate as a cistronic cluster at 13q14, is deleted or decreased in most cases (approx. 68%) of B cell chronic lymphocytic leukemia (B-CLL) (6). Both these miRNAs negatively regulate the expression of B cell lymphoma 2 (Bcl2), that is reported to be expressed in many types of cancer including leukemias, and inhibit cell death (7). Overexpression of miR-15 and miR-16 in the MEG-01 cell line actually induces the apoptosis. Inversely, one cluster of miRNAs, miR-17 – 92 polycistron, was found to increase in the cancers such as B-CLL (8). The expression of six miRNAs in this cluster is upregulated by c-myc, whose expression and/or function are one of the most common abnormalities in human cancers, and miR-17-5p and miR-20a included in this cluster negatively regulate the expression of transcriptional factor E2F1 (9). Furthermore, mice reconstituted with hemotopoietic stem cells overexpressing miR-17 – 19b exhibit accelerated c-myc-induced lymphomagenesis (8). Furthermore, it was revealed that miRNA expression profiles enable researchers to successfully classify poorly characterized human tumors that can not be accurately classified by mRNA expression profiles (10). These results show the possibility that miRNAs have clinical benefits as not only therapeutic targets but also a tool for cancer diagnosis.
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